Kotaro Nochioka1,2, Candida Cristina Quarta3,4, Brian Claggett1, Gabriela Querejeta Roca1, Claudio Rapezzi4, Rodney H Falk5, Scott D Solomon1. 1. Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street Boston, MA 02115, USA. 2. Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Clinical Research, Innovation and Education Center, Tohoku University Hospital, Seiryo-machi 1-1 Aobaku Sendai, Miyagi 980-8574, Japan. 3. Division of Medicine, National Amyloidosis Centre UCL, Royal Free Hospital, Rowland Hill Street, London NW3 2PF, UK. 4. Cardiology, Department of Experimental Diagnostic and Specialty Medicine, Alma Mater Studiorum University of Bolonga, PAD 21,Policlinico S.Orsola-Malpighi, via Massarenti 9, 40138 Bologna, Italy. 5. Department of Cardiology, Harvard Vanguard Medical Associates, Brigham and Women's Hospital Cardiac Amyloidosis Program, Harvard Medical School, 75 Francis Street Boston, MA 02115, USA.
Abstract
AIMS: Although cardiac amyloidosis (CA) is characterized by significant left atrial (LA) dilatation, the characteristics of LA function remain to be fully investigated. METHODS AND RESULTS: We assessed LA function by speckle-tracking echocardiography in 124 patients with CA and sinus rhythm: 68 with light chain (AL), 29 with mutant (ATTRm), 27 with wild-type (ATTRwt) transthyretin amyloidosis. Conventional and strain-derived parameters, including LA peak longitudinal strain (LS) and strain rate (peak LSR: reservoir function; early LSR: conduit function; late LSR: active function), were assessed compared between CA patients and 20 healthy controls of similar age and gender. All LA function phases, including LA longitudinal strain, peak LSR, early and late LSR were significantly impaired in CA compared to healthy controls after adjusting for LA size, LV ejection fraction and LV filling pressures (E/E') (all P < 0.05). Peak LA LS was moderately correlated with LV global LS (R = -0.60, P < 0.001); late LSR was correlated with A wave at the level of LV inflow (R = -0.69, P < 0.001). Among the different CA subtypes, peak LS and LA active emptying fraction were worse in ATTRwt than AL and ATTRm [P < 0.05 after adjustment for age, sex, body mass index, systolic blood pressure, heart rate, LA volume index, severity of mitral regurgitation, left ejection fraction, and left ventricular end-diastolic pressure (E/E')]. CONCLUSION: In CA, LA function was severely impaired and highly correlated with LV deformation. Differences in LA function between amyloid subtypes suggest that amyloid aetiology plays a role in the pathophysiology of cardiac dysfunction in CA. Published on behalf of the European Society of Cardiology. All rights reserved.
AIMS: Although cardiac amyloidosis (CA) is characterized by significant left atrial (LA) dilatation, the characteristics of LA function remain to be fully investigated. METHODS AND RESULTS: We assessed LA function by speckle-tracking echocardiography in 124 patients with CA and sinus rhythm: 68 with light chain (AL), 29 with mutant (ATTRm), 27 with wild-type (ATTRwt) transthyretin amyloidosis. Conventional and strain-derived parameters, including LA peak longitudinal strain (LS) and strain rate (peak LSR: reservoir function; early LSR: conduit function; late LSR: active function), were assessed compared between CA patients and 20 healthy controls of similar age and gender. All LA function phases, including LA longitudinal strain, peak LSR, early and late LSR were significantly impaired in CA compared to healthy controls after adjusting for LA size, LV ejection fraction and LV filling pressures (E/E') (all P < 0.05). Peak LA LS was moderately correlated with LV global LS (R = -0.60, P < 0.001); late LSR was correlated with A wave at the level of LV inflow (R = -0.69, P < 0.001). Among the different CA subtypes, peak LS and LA active emptying fraction were worse in ATTRwt than AL and ATTRm [P < 0.05 after adjustment for age, sex, body mass index, systolic blood pressure, heart rate, LA volume index, severity of mitral regurgitation, left ejection fraction, and left ventricular end-diastolic pressure (E/E')]. CONCLUSION: In CA, LA function was severely impaired and highly correlated with LV deformation. Differences in LA function between amyloid subtypes suggest that amyloid aetiology plays a role in the pathophysiology of cardiac dysfunction in CA. Published on behalf of the European Society of Cardiology. All rights reserved.
Authors: Sharmila Dorbala; Yukio Ando; Sabahat Bokhari; Angela Dispenzieri; Rodney H Falk; Victor A Ferrari; Marianna Fontana; Olivier Gheysens; Julian D Gillmore; Andor W J M Glaudemans; Mazen A Hanna; Bouke P C Hazenberg; Arnt V Kristen; Raymond Y Kwong; Mathew S Maurer; Giampaolo Merlini; Edward J Miller; James C Moon; Venkatesh L Murthy; C Cristina Quarta; Claudio Rapezzi; Frederick L Ruberg; Sanjiv J Shah; Riemer H J A Slart; Hein J Verberne; Jamieson M Bourque Journal: J Nucl Cardiol Date: 2019-12 Impact factor: 5.952
Authors: Karen Rausch; Gregory M Scalia; Kei Sato; Natalie Edwards; Alfred King-Yin Lam; David G Platts; Jonathan Chan Journal: Int J Cardiovasc Imaging Date: 2020-07-29 Impact factor: 2.357
Authors: Francesco Bandera; Anita Mollo; Matteo Frigelli; Giulia Guglielmi; Nicoletta Ventrella; Maria Concetta Pastore; Matteo Cameli; Marco Guazzi Journal: Front Cardiovasc Med Date: 2022-01-13